Embolic stroke is the nation's third leading killer, and is a major cause of disability. There are over 780,000 strokes per year in the United States alone. Of these, roughly 110,000 are hemorrhagic, and 670,000 are ischemic (either due to vessel narrowing or to embolism). The most common cause of ischemic stroke of cardiac origin is thromboemboli due to atrial fibrillation. One out of every six strokes (approximately 130,000 per year) is attributed to atrial fibrillation. Atrial fibrillation is the most common heart arrhythmia; it results in a rapid and chaotic heartbeat that lowers cardiac output and leads to irregular and turbulent blood flow in the vascular system. There are over eight million people worldwide with atrial fibrillation, with about eight hundred thousand new cases reported each year. Atrial fibrillation is associated with a 500 percent greater risk of stroke compared with age-matched healthy controls. A patient with atrial fibrillation typically has a significantly decreased quality of life due, in part, to the fear of stroke, and the pharmaceutical regimen necessary to reduce that risk.
When patients develop atrial thrombus from atrial fibrillation, the clot occurs in or originates from the left atrial appendage (LAA) of the heart over ninety percent of the time. The left atrial appendage is a closed cavity which looks like a small thumb or windsock; it is connected to the anterolateral wall of the left atrium between the mitral valve and the root of the left pulmonary vein. The left atrial appendage contracts with the left atrium during a normal heart cycle, thus keeping blood from becoming stagnant. However, with atrial fibrillation, the left atrial appendage often fails to contract with any vigor due to the disorganized electrical signals. As a result, thrombus formation is predisposed to form in the stagnant blood within the left atrial appendage.
Pharmacological therapies for stroke prevention in atrial fibrillation patients such as oral or systemic administration of warfarin have often been inadequate due to serious side effects and lack of patient compliance. Invasive surgical or thorascopic techniques have been used to obliterate the left atrial appendage, however, many patients are not suitable candidates for such procedures due to compromised condition or previous cardiac surgery. In addition, the perceived risks of these surgical procedures often outweigh the potential benefits.
Many of the current commercial devices that attempt to occlude the left atrial appendage for stroke prevention in atrial fibrillation patients utilize a rigid, cylindrical support frame with tissue-piercing fixation members and macroporous filtering membranes that allow the passage of blood. These devices have a number of issues and/or potential drawbacks. The opening (ostium) of the left atrial appendage varies in geometry and size. Sealing the left atrial appendage with a rigid frame that presupposes a circular ostium can be less effective at preventing thromboemboli from entering systemic circulation.
Securing a device in the left atrial appendage is a major safety concern to physicians. Many of the current left atrial appendage occlusion or filtering devices employ tissue-piercing fixation members. The tissue of the left atrial appendage is generally fragile and thin. The heart is encased in a tough, non-elastic pericardial sac. This makes bleeding from the heart through the holes caused by the tissue-piercing fixation members into the pericardial space a potentially life-threatening situation due to the potential for tamponade (compression of the heart when blood or fluid builds up in the space between the myocardium (heart muscle) and the pericardium (outer covering sac of the heart)).
Another concern with many of the current devices is the filtering type membranes. These membranes are macroporous and do not provide immediate cessation of blood flow through the membrane. Such membranes can take hours to weeks to substantially occlude. The possibility exists for thromboemboli to enter the blood stream while the clotting/occluding process of the filtering membrane takes place. Many of these atrial fibrillation patients are on some type of blood thinning (anticoagulant or antiplatelet) medication, which could prolong the clotting/occluding process for these filtering membranes and expose patients to stroke risk.